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Neuro 2 Flashcards

1
Q

A patient is brought in because of memory loss, shuffling gait, masklike facies, akinesia, rigidity, and a resting tremor. What is likely going on? What caused it?

A

Parkinson disease

Idiopathic dopamine depletion
Loss of dopaminergic striated neurons in the substantia nigra
Lew body (eosinophilic cytoplasmic inclusions in neurons) formation --> abnormal cholinergic input to cortex
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2
Q

How is parkinson disease treated?

A

Dopaminergic agonists (levodopa, carbidopa, bromocriptine, amantadine)
MAO-B inhibitors (selegiline)
Anticholinergic agents (benztropine)
Amantadine

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3
Q

How does levodopa work? When is it used? What are significant side effects?

A

Dopamine precursor

Initial therapy

Hallucinations
Mood changes
Dyskinesia with chronic use

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4
Q

How does carbidopa work? When is it used? What are significant side effects?

A

Dopamine decarboxylase inhibitor that reduces levodopa metabolism

To augment levodopa

Reduces adverse effects of levodopa by allowing smaller dosage

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5
Q

How does bromocriptine work? What are significant side effects?

A

Dopamine receptor antagonist

Increases response to levodopa

Hallucinations, confusion, hypotension, cardiotoxicity

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6
Q

When is selegiline used? What are significant side effects?

A

Early disease…may delay need to start levodopa

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7
Q

How does amantadine work? When is it used? What are significant side effects?

A

Increase synthesis, release, or repute of dopamine

For rigidity and bradykinesia

Agitation, hallucinations

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8
Q

What is necessary to diagnose ALS? How is it treated?

A

Lower motor neuron signs in at least 2 extremities AND upper motor neuron signs in one region

Riluzole may slow progression

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9
Q

A patient comes in with motor and mental dysfunction starting in middle age. Dad had similar symptoms before he died. What would be seen on genetic analysis? CT or MRI?

A

CAG repeats on chromosome 4…because this is Huntington disease

Caudate nucleus and putamen atrophy

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10
Q

How is Huntington disease treated?

A

Dopamine antagonist may improve chorea (haloperidol)

Tetrabenazine and reserpine inhibit vesicular monamine transport…limits how much dopamine gets packaged/released

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11
Q

What causes alzheimer disease?

A

Neurofibrillary tangles
Neuritic plaques
Amyloid deposition
Neuronal atrophy

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12
Q

What is seen on CT or MRI with alzheimer disease? How is it treated?

A

Cortical atrophy

Cholinesterase inhibitors (donepezil, rivastigmine, galantamine)
Memantine
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13
Q

Patient has come in because she has had many random things that will bother her, then go away, and then something else will bother her…often it’s her vision. What is likely seen on LP? MRI?

A

This is MS:
LP shows increased protein, mildly increased WBCs, oligoclonal bands*, increased IgG

Asymmetric white matter lesions

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14
Q

How is MS treated?

A

Corticosteroids, methotrexate, avoidance of stress –> decrease length of exacerbations

Interferon-beta and glatiramer acetate –> decrease frequency of exacerbations

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15
Q

What causes syringomyelia? How is it treated?

A

Post-traumatic cystic degeneration of spinal cord from unknown mechanism (takes years) –> syrinx cavity expands and compresses adjacent neural tissue

Surgery…shunting if recurrent

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16
Q

A young woman comes in with periodic weakness and muscle fatigue that gets worse throughout the day, ptosis, diplopia, and dysarthria. What is this? What caused this? What is it associated with?

A

Myasthenia gravis

Antibodies bind to post-synaptic ACh receptors –> blocking normal neuromuscular transmission –> easy fatigue

Thymoma and thyrotoxicosis (get a chest CT after diagnosis)

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17
Q

How is myasthenia gravis diagnosed? Treated?

A

Edrophonium…a short acting anti cholinesterase

Anticholinesterase agents (neostigmine, pyridostigmine)
Thymectomy
Immunosuppressive agents
Plasmapheresis
IVIG for refractory cases
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18
Q

A patient is diagnosed with, or likely has, SCLC and presents just like myasthenia gravis. What could this possibly be? How is it treated?

A

Lambert-Eaton syndrome…antibodies form to presynaptic calcium channels

Immunosuppression
Plasmapheresis

19
Q

A patient comes in after a recent viral illness with bilateral weakness in distal extremities with decreased sensation on exam. What is likely going on? What would be seen on LP? How is it treated?

A

Guillain-Barre syndrome

Increased protein, normal glucose and pressure

Self-resolves…plasmapheresis or IVIG can speed it up

20
Q

A person comes in concerned about a fixed oscillation of hands or head. What is this called? What is it associated with? How is it treated?

A

Benign Essential Tremor

Idiopathic

beta-blockers, primidone, or clonazepam
Thalatomy or deep brain stimulation in refractory cases

21
Q

Patient comes in with rapid flinching of distal limb and abnormal facial movements. What is it? What is it associated with?

A

Chorea

Hyperthyroidism, stroke, Huntington disease, SLE, levodopa use, rheumatic fever

22
Q

Patient comes in with writhing, snakelike movement in extremities. What is it? What is it associated with?

A

Athetosis

Cerebral palsy, encephalopathy, Huntington disease, Wilson disease

23
Q

Patient comes in with sustained proximal limb and trunk contractions. What is it? What is it associated with? How can it be treated?

A

Dystonia

Wilson disease, Parkinson disease, Huntington disease, encephalitis, neuroleptic use (tardive dyskinesia)

Carbidopa, levodopa, botulinum toxin…treat underlying disorder

24
Q

Patient comes in with flinging of proximal extremities. What is it? What is it associated with? How is it treated?

A

Hemiballismus

Stroke (subthalamic nucleus)

Haloperidol

25
Q

Patient comes in because s/he makes brief involuntary movements or sounds. What is this? what is it associated with? How is it treated?

A

Tics

Tourette syndrome, OCD, ADHD

Fluphenazine, pimozide, tetrabenazine

26
Q

What is the most common primary brain tumor in adults? Where do they tend to be?

A

Glioblastoma (meningioma and schwannoma round out top 3)

Supratentorial

27
Q

What is the most primary brain tumor in kids? Where do they tend to be?

A

Astrocytoma (medulloblastoma [malignant] and ependymoma [may be malignant] round out top 3)

Infratentorial

28
Q

How is Neurfibromatosis type I diagnosed?

A

COFFINS

C- Cafe-au-lait spot b/w 5-15mm
O- Optic glioma
F- Freckling of axillary or inguinal area
F- Family history (1st degree relative)
I- Iris hamartomas more than 1 (Lisch nodules
N- Neurofibromas more than 1 or plexiform neurofibroma (tumors with mix of Schwann cells, fibroblasts, and mast cells)
S-Skeletal lesions (cortical thinning of long bones, sphenoid dysplasia)

29
Q

How is hypersomnia (sudden occurrence of sleep) treated?

A

Modafinil*
Methylphenidate
Pemoline

30
Q

How is cataplexy (sudden loss of muscle tone) treated?

A

TCAs

31
Q

What do benzos do to the quality of sleep?

A

Decrease N3 and increase N2…do not reproduce normal sleep architecture

32
Q

What is ‘persistent vegetative state’?

A

Normal sleep cycles
Inability to perceive and interact wit environment
Preserved autonomic function

33
Q

Patient is in a coma with large, nonreactive pupils. What is possible cause? Small reactive pupils? Pinpoint pupils?

A

Damage below midbrain (CN III involvement; possible uncal herniation)

Thalamic involvement, transtentorial herniation

Opioid OD; toxic effect

34
Q

Patient is in a coma with immobile, reactive eyes. What is possible cause? Doll’s eyes?

A

Metabolic cause

Intact brainstem

35
Q

Patient is in a coma and you do a cold water caloric reflex test. Conjugate deviation toward that ear? No abduction/adduction? Conjugate nystagmus?

A

Intact midbrain

CN VI and III involvement

Psychogenic cause

36
Q

Patient is in a coma and has spastic paralysis. Where is the injury? Decorticate posturing (elbows flexed, legs extended)? Decerebrate posturing (elbows and legs extended)? No response to painful stimuli? Appropriate pain response?

A

High spinal cord injury

Cortical or thalamic compression

Midbrain involvement

Pontine, medullary involvement

Superficial cause (not deep brain)

37
Q

Where is the obstruction in noncommunicating hydrocephalus? Communicating hydrocephalus?

A

4th cerebral ventricle

Dysfunction of subarachnoid cisterns or arachnoid villi

38
Q

What medications can be used to relieve symptoms of hydrocephalus? What is long term management and what is a possible side effect?

A

Acetazolamide or furosemide

Shunting…increases risk of meningitis

39
Q

What enzyme is absent with Tay-Sachs?

A

Hexosaminidase A

40
Q

What will be elevated during maternal screening if the child has a neural tube defect?

A

Alpha-fetoprotein

Acetylcholinesterase

41
Q

There are two types of cerebral palsy. What causes spastic CP? What else is often seen in these patients?

A

Damage of pyramidal tracts

Mental retardation

42
Q

There are two types of cerebral palsy. What causes dyskinetic CP?

A

Extrapyramidal pathology

43
Q

A baby is found to have leukocoria. What is this? What does it mean? What caused it?

A

Poor red reflex or white retinal mass

Retinoblastoma (malignant)…caused by RBI mutation

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